[1]田甜,沈山梅.肠促胰素与骨质疏松[J].国际内分泌代谢杂志,2016,36(05):320-322.[doi:10.3760/cma.j.issn.1673-4157.2016.05.09]
 Tian Tian,Shen Shanmei.Incretin and osteoporosis[J].International Journal of Endocrinology and Metabolism,2016,36(05):320-322.[doi:10.3760/cma.j.issn.1673-4157.2016.05.09]
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肠促胰素与骨质疏松()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
36
期数:
2016年05期
页码:
320-322
栏目:
综述
出版日期:
2016-09-20

文章信息/Info

Title:
Incretin and osteoporosis
作者:
田甜沈山梅
210009 南京,东南大学医学院(田甜,沈山梅); 210008 南京大学医学院附属鼓楼医院内分泌科(沈山梅)
Author(s):
Tian TianShen Shanmei
Department of Endocrinology, DrumTower Hospital Affiliated to Nanjing University Medical School,Nanjing 210009,China
关键词:
骨质疏松 胰高血糖素样肽-1 胰高血糖素样肽-2 葡萄糖依赖性促胰岛素多肽
Keywords:
Osteoporosis Glucagon-like peptide-1 Glucagon-like peptide-2 Glucose-dependent insulinotropic peptide
DOI:
10.3760/cma.j.issn.1673-4157.2016.05.09
摘要:
正常人体骨量的维持依赖于成骨细胞新骨生成与破骨细胞骨吸收的骨重建过程。凡是能增加骨吸收、减少骨生成的因素均能使骨密度降低,进而发生骨质疏松。肠促胰素主要由胰高血糖素样肽(GLP)和葡萄糖依赖性促胰岛素多肽(GIP)组成。最新研究发现,GIP及GLP-1均能抑制骨吸收过程,同时促进骨的生成,而目前的研究显示,GLP-2仅对骨吸收有抑制作用。
Abstract:
Normal human bone mass is maintained by the process of bone remodeling,including bone formation and bone resorption. Factors which increase bone resorption and reduce bone formation could reduce bone mineral density, and thus resulting in osteoporosis.Incretin is secreted by the intestinal cells, which can stimulate insulin secretion and regulate glycometabolism.Incretin includes glucagon-like peptide(GLP), and glucose-dependent insulinotropic polypeptide(GIP). GIP and GLP-1 can inhibit bone resorption, while promoting bone formation, and the current study shows that GLP-2 only inhibits bone resorption.

参考文献/References:

[1] Clowes JA,Hannon RA,Yap TS,et al.Effect of feeding on bone turnover markers and its impact on biological variability of measurements[J]. Bone,2002,30(6):886-890. DOI: 10.1016/S8756-3282(02)00728-7.
[2] Mabilleau G, Mieczkowska A, Chappard D.Use of glucagon-like peptide-1 receptor agonists and bone fractures: a meta-analysis of randomized clinical trials[J]. Diabetes, 2014,6(3):260-266. DOI: 10.1111/1753-0407.12102.
[3] Su B, Sheng H, Zhang M,et al.Risk of bone fractures associated with glucagon-like peptide-1 receptor agonists' treatment: a meta-analysis of randomized controlled trials[J]. Endocrine, 2015,48(1):107-115. DOI: 10.1007/s12020-014-0361-4.
[4] Irwin N, Flatt PR.New perspectives on exploitation of incretin peptides for the treatment of diabetes and related disorders[J]. World J Diabetes, 2015,6(15):1285-1295. DOI: 10.4239/wjd.v6.i15.1285.
[5] Bjerre Knudsen L, Madsen LW, Andersen S,et al. Glucagon-like peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin relerse and C-cell proliferation[J].Endocrinology,2010,151(4):1473-1486. DOI: 10.1210/en.2009-1272.
[6] Nuche-Berenguer B, Moreno P, Portal-Nunez S, et al. Exendin-4 exerts osteogenic action in insulin-resistant and type 2diabetic states[J]. Regul Pept, 2010, 159(1-3):61-66. DOI: 10.1016/j.regpep.2009.06.010.
[7] Yamada C, Yamada Y, Tsukiyamak K, et al. The murine glucagon-like peptide-1 receptor is essential for control of bone resorption[J].Endocrinology, 2008,149(2):574-579. DOI: 10.1210/en.2007-1292.
[8] Nuche-Berenguer B,Lozano D,Gutiérrez-Rojas I,et a1. GLP-1 and exendin-4 can reverse hyperlipidic-related osteopenia[J].J Endocrinol,2011,209(2):203-210.DOI: 10.1530/JOE-11-0015.
[9] Ma X, Meng J, Jia M,et al. Exendin-4, a glucagon-like peptide-1 receptor agonist, prevents osteopenia by promoting bone formation and suppressing bone resorption in aged ovariectomized rats[J]. J Bone Miner Res, 2013,28(7):1641-1652. DOI: 10.1002/jbmr.1898.
[10] Jeon YK, Bae MJ, Kim JI,et al. Expression of Glucagon-Like Peptide 1 Receptor during Osteogenic Differentiation of Adipose-Derived Stem Cells[J]. Endocrinol Metab(Seoul),2014,29(4):567-573. DOI: 10.3803/EnM.2014.29.4.567.
[11] Drucker DJ, Yusta B.Physiology and pharmacology of the enteroendocrine hormone glucagon-like peptide-2[J]. Annu Rev Physiol, 2014,76: 561-583. DOI: 10.1146/annurev-physiol-021113-170317.
[12] Lopes LS, Schwartz RP, Ferraz-de-Souza B. et al. The role of enteric hormone GLP-2 in the response of bone markers to a mixed meal in postmenopausal women with type 2 diabetes mellitus[J]. Diabetol Metab Syndr, 2015,7:13.DOI:10.1186/s13098-015-0006-7.
[13] Henriksen DB, Alexandersen P, Hartmann B, et al. Four-month treatment with GLP-2 significantly increases hip BMD: a randomized, placebo-controlled, dose-ranging study in postmenopausal women with low BMD[J]. Bone.2009; 45(5):833-842.DOI: 10.1016/j.bone.2009.07.008.
[14] Walsh JS, Henriksen DB. Feeding and bone[J]. Arch Biochem Biophys, 2010,503(1):11-19. DOI: 10.1016/j.abb.2010.06.020.
[15] Holst JJ, Hartmann B, Gottschalck IB,et al. Bone resorption is decreased postprandially by intestinal factors and glucagon-like peptide-2 is a possible candidate[J]. Scand J Gastroenterol, 2007,42(7):814-820. DOI: 10.1080/00365520601137272.
[16] Askov-Hansen C, Jeppesen PB, Lund P. et al. Effect of glucagon-like peptide-2 exposure on bone resorption: effectiveness of high concentration versus prolonged exposure[J]. Regul Pept, 2013, 181:4-8. DOI: 10.1016/j.regpep.2012.11.002.
[17] Mieczkowska A, Irwin N, Flatt PR, et al. Glucose-dependent insulinotropic polypeptide(GIP)receptor deletion leads to reduced bone strength and quality[J]. Bone,2013,56(2):337-342. DOI: 10.1016/j.bone.2013.07.003.
[18] Torekov SS, Harsløf T, Rejnmark L,et al. A functional amino acid substitution in the glucose-dependent insulinotropic polypeptide receptor(GIPR)gene is associated with lower bone mineral density and increased fracture risk[J]. J Clin Endocrinol Metab, 2014,99(4):E729-E733. DOI: 10.1210/jc.2013-3766.
[19] Mabilleau G, Mieczkowska A, Irwin N,et al. Beneficial effects of a N-terminally modified GIP agonist on tissue-level bone material properties[J].Bone,2014,63:61-68.DOI: 10.1016/j.bone.2014.02.013.
[20] Kanazawa I. Updates on Lifestyle-Related Diseases and Bone Metabolism. The relationship between incretin and bone metabolism[J].Clin Calcium,2014,24(11):1671-1677.DOI: CliCa141116711677.
[21] Mieczkowska A, Bouvard B, Chappard D,et al. Glucose-dependent insulinotropic polypeptide(GIP)directly affects collagen fibril diameter and collagen cross-linking in osteoblast cultures[J]. Bone,2015,74:29-36. DOI: 10.1016/j.bone.2015.01.003.
[22] Mabilleau G, Mieczkowska A, Irwin N,et al. Beneficial effects of a N-terminally modified GIP agonist on tissue-level bone material properties[J].Bone,2014,63:61-68.DOI: 10.1016/j.bone.2014.02.013.

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备注/Memo

备注/Memo:
通信作者:沈山梅,Email:shanmeishen@126.com
更新日期/Last Update: 2016-11-20